The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis
Glioblastoma (GBM) is the most aggressive and malignant primary tumor. Angiogenesis plays a critical role in the progression of GBM. Previous studies have indicated that long non-coding RNAs (lncRNAs) are abnormally expressed in various cancers and participate in the regulation of the malignant beha...
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| Format: | Article |
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Frontiers Media S.A.
2018-01-01
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| Series: | Frontiers in Molecular Neuroscience |
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| Online Access: | http://journal.frontiersin.org/article/10.3389/fnmol.2017.00437/full |
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| author | Chunqing Yang Chunqing Yang Chunqing Yang Jian Zheng Jian Zheng Jian Zheng Yixue Xue Yixue Xue Hai Yu Hai Yu Hai Yu Xiaobai Liu Xiaobai Liu Xiaobai Liu Jun Ma Jun Ma Libo Liu Libo Liu Ping Wang Ping Wang Zhen Li Zhen Li Zhen Li Heng Cai Heng Cai Heng Cai Yunhui Liu Yunhui Liu Yunhui Liu |
| author_facet | Chunqing Yang Chunqing Yang Chunqing Yang Jian Zheng Jian Zheng Jian Zheng Yixue Xue Yixue Xue Hai Yu Hai Yu Hai Yu Xiaobai Liu Xiaobai Liu Xiaobai Liu Jun Ma Jun Ma Libo Liu Libo Liu Ping Wang Ping Wang Zhen Li Zhen Li Zhen Li Heng Cai Heng Cai Heng Cai Yunhui Liu Yunhui Liu Yunhui Liu |
| author_sort | Chunqing Yang |
| collection | DOAJ |
| description | Glioblastoma (GBM) is the most aggressive and malignant primary tumor. Angiogenesis plays a critical role in the progression of GBM. Previous studies have indicated that long non-coding RNAs (lncRNAs) are abnormally expressed in various cancers and participate in the regulation of the malignant behaviors of tumors. The present study demonstrated that lncRNA antisense 1 to Micro-chromosome maintenance protein 3-associated protein (MCM3AP-AS1) was upregulated whereas miR-211 was downregulated in glioma-associated endothelial cells (GECs). Knockdown of MCM3AP-AS1 suppressed the cell viability, migration, and tube formation of GECs and played a role in inhibiting angiogenesis of GBM in vitro. Furthermore, knockdown of MCM3AP-AS1 increased the expression of miR-211. Luciferase reporter assay implicated that miR-211 targeted KLF5 3′-UTR and consequently inhibited KLF5 expression. Besides, in this study we found that MCM3AP-AS1 knockdown decreased KLF5 and AGGF1 expression by upregulating miR-211. In addition, KLF5 was associated with the promoter region of AGGF1. Knockdown of KLF5 decreased AGGF1 expression by transcriptional repression, and also inhibited the activation of PI3K/AKT and ERK1/2 signaling pathways. Overall, this study reveals that MCM3AP-AS1/miR-211/KLF5/AGGF1 axis plays a prominent role in the regulation of GBM angiogenesis and also serves as new therapeutic target for the anti-angiogenic therapy of glioma. |
| first_indexed | 2024-12-13T17:06:03Z |
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| institution | Directory Open Access Journal |
| issn | 1662-5099 |
| language | English |
| last_indexed | 2024-12-13T17:06:03Z |
| publishDate | 2018-01-01 |
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| series | Frontiers in Molecular Neuroscience |
| spelling | doaj.art-eb8b3cf592fb443d81084017b73cab4d2022-12-21T23:37:41ZengFrontiers Media S.A.Frontiers in Molecular Neuroscience1662-50992018-01-011010.3389/fnmol.2017.00437316485The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma AngiogenesisChunqing Yang0Chunqing Yang1Chunqing Yang2Jian Zheng3Jian Zheng4Jian Zheng5Yixue Xue6Yixue Xue7Hai Yu8Hai Yu9Hai Yu10Xiaobai Liu11Xiaobai Liu12Xiaobai Liu13Jun Ma14Jun Ma15Libo Liu16Libo Liu17Ping Wang18Ping Wang19Zhen Li20Zhen Li21Zhen Li22Heng Cai23Heng Cai24Heng Cai25Yunhui Liu26Yunhui Liu27Yunhui Liu28Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, ChinaLiaoning Research Center for Clinical Medicine in Nervous System Disease, Shenyang, ChinaKey Laboratory of Neuro-oncology in Liaoning Province, Shenyang, ChinaDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, ChinaLiaoning Research Center for Clinical Medicine in Nervous System Disease, Shenyang, ChinaKey Laboratory of Neuro-oncology in Liaoning Province, Shenyang, ChinaDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, ChinaKey Laboratory of Cell Biology, Ministry of Public Health of China, and Key Laboratory of Medical Cell Biology, Ministry of Education of China, Shenyang, ChinaDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, ChinaLiaoning Research Center for Clinical Medicine in Nervous System Disease, Shenyang, ChinaKey Laboratory of Neuro-oncology in Liaoning Province, Shenyang, ChinaDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, ChinaLiaoning Research Center for Clinical Medicine in Nervous System Disease, Shenyang, ChinaKey Laboratory of Neuro-oncology in Liaoning Province, Shenyang, ChinaDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, ChinaKey Laboratory of Cell Biology, Ministry of Public Health of China, and Key Laboratory of Medical Cell Biology, Ministry of Education of China, Shenyang, ChinaDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, ChinaKey Laboratory of Cell Biology, Ministry of Public Health of China, and Key Laboratory of Medical Cell Biology, Ministry of Education of China, Shenyang, ChinaDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, ChinaKey Laboratory of Cell Biology, Ministry of Public Health of China, and Key Laboratory of Medical Cell Biology, Ministry of Education of China, Shenyang, ChinaDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, ChinaLiaoning Research Center for Clinical Medicine in Nervous System Disease, Shenyang, ChinaKey Laboratory of Neuro-oncology in Liaoning Province, Shenyang, ChinaDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, ChinaLiaoning Research Center for Clinical Medicine in Nervous System Disease, Shenyang, ChinaKey Laboratory of Neuro-oncology in Liaoning Province, Shenyang, ChinaDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, ChinaLiaoning Research Center for Clinical Medicine in Nervous System Disease, Shenyang, ChinaKey Laboratory of Neuro-oncology in Liaoning Province, Shenyang, ChinaGlioblastoma (GBM) is the most aggressive and malignant primary tumor. Angiogenesis plays a critical role in the progression of GBM. Previous studies have indicated that long non-coding RNAs (lncRNAs) are abnormally expressed in various cancers and participate in the regulation of the malignant behaviors of tumors. The present study demonstrated that lncRNA antisense 1 to Micro-chromosome maintenance protein 3-associated protein (MCM3AP-AS1) was upregulated whereas miR-211 was downregulated in glioma-associated endothelial cells (GECs). Knockdown of MCM3AP-AS1 suppressed the cell viability, migration, and tube formation of GECs and played a role in inhibiting angiogenesis of GBM in vitro. Furthermore, knockdown of MCM3AP-AS1 increased the expression of miR-211. Luciferase reporter assay implicated that miR-211 targeted KLF5 3′-UTR and consequently inhibited KLF5 expression. Besides, in this study we found that MCM3AP-AS1 knockdown decreased KLF5 and AGGF1 expression by upregulating miR-211. In addition, KLF5 was associated with the promoter region of AGGF1. Knockdown of KLF5 decreased AGGF1 expression by transcriptional repression, and also inhibited the activation of PI3K/AKT and ERK1/2 signaling pathways. Overall, this study reveals that MCM3AP-AS1/miR-211/KLF5/AGGF1 axis plays a prominent role in the regulation of GBM angiogenesis and also serves as new therapeutic target for the anti-angiogenic therapy of glioma.http://journal.frontiersin.org/article/10.3389/fnmol.2017.00437/fullangiogenesisglioblastomaMCM3AP-AS1miR-211KLF5AGGF1 |
| spellingShingle | Chunqing Yang Chunqing Yang Chunqing Yang Jian Zheng Jian Zheng Jian Zheng Yixue Xue Yixue Xue Hai Yu Hai Yu Hai Yu Xiaobai Liu Xiaobai Liu Xiaobai Liu Jun Ma Jun Ma Libo Liu Libo Liu Ping Wang Ping Wang Zhen Li Zhen Li Zhen Li Heng Cai Heng Cai Heng Cai Yunhui Liu Yunhui Liu Yunhui Liu The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis Frontiers in Molecular Neuroscience angiogenesis glioblastoma MCM3AP-AS1 miR-211 KLF5 AGGF1 |
| title | The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis |
| title_full | The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis |
| title_fullStr | The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis |
| title_full_unstemmed | The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis |
| title_short | The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis |
| title_sort | effect of mcm3ap as1 mir 211 klf5 aggf1 axis regulating glioblastoma angiogenesis |
| topic | angiogenesis glioblastoma MCM3AP-AS1 miR-211 KLF5 AGGF1 |
| url | http://journal.frontiersin.org/article/10.3389/fnmol.2017.00437/full |
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